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The binding of 125I-labelled anti-bovine serum albumin (BSA)-BSA immune complexes (IC), giving a final molar antibody to antigen ratio of 1:1, to monocytes isolated from 18 patients with systemic lupus erythematosus (SLE) and from 10 normal healthy donors was quantitatively investigated. The degradation of the bound IC by the same monocytes was kinetically determined at the same time. The assays were performed on monocyte monolayers. Scatchard plots at 4 degrees C demonstrated that monocytes from patients with active SLE expressed a mean Fc gamma receptor (FcR) number that was 22% higher than that of the controls, although this did not reach statistical significance. The FcR number of normal monocytes and the degradation rate of anti-BSA-BSA complexes by the same cells showed a positive correlation. At the same time, the digestion of anti-BSA-BSA complexes by monocytes of SLE patients with active disease was prolonged, despite their enhanced FcR-ligand binding. The dissociation of FcR-ligand binding and FcR-mediated degradation suggests that the IC degradation is controlled by altered biochemical mechanisms in the monocytes of SLE patients.

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Follow-up immunological studies in 27 patients with acute pancreatitis of known etiology showed a significant elevation in the level of circulating immune complexes (IC), a significant inhibition in migration of leukocytes (with direct LMT) of patients and a significant decrease in the percentage of T-active, T-total peripheral lymphocytes and in the absolute count of peripheral T cells. .Elevated circulating IC levels could been detected 3-4 weeks after the onset of acute pancreatitis. These immunological changes have still been demonstrated in a number of patients 7–14 months after recovery. We have found similar immunological alterations in patients with chronic pancreatitis as well. The possible causes and role of these long-term existing immunologic abnormalities are discussed.

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